Organic Phosphorous Compound and Carbamate Toxicity Treatment & Management

Updated: Dec 29, 2016
  • Author: Daniel K Nishijima, MD, MAS; Chief Editor: Asim Tarabar, MD  more...
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Approach Considerations

Identification of the type of chemical is important in determining the patient's clinical course and prognosis. Emergency Medical Service (EMS) personnel should attempt to bring in the labels or the names of chemicals the patient was exposed to because different organophosphorous compounds (OPCs) have different aging and reactivation times, which may help in guiding treatment. As a general rule, dimethyl OPCs undergo rapid aging, which makes early initiation of oximes critical. In comparison, diethyl compounds may cause delayed toxicity, and oxime therapy may need to be prolonged. [18]


Emergency Department Care

Emergency department (ED) treatment measures include the following:

  • Airway, breathing, and circulation (ABCs)
  • Decontamination
  • Atropine
  • Oximes
  • Other treatments


Care of the ABCs should be initiated first. Providers with appropriate personal protective equipment (PPE) can address the ABCs before decontamination.

Intubation may be necessary in cases of severe poisoning. Because succinylcholine is metabolized by means of plasma cholinesterase, OPC or carbamate poisoning may cause prolonged paralysis. Increased doses of nondepolarizing agents, such as pancuronium or vecuronium, may be required to achieve paralysis because of the excess acetylcholine (ACh) at the receptor. [14]


Decontamination is an important part of the initial care. In general, the importance of decontamination depends on the route of poisoning. Patients with dermal and inhalation poisonings must be decontaminated before being brought into the ED if it was not done in the prehospital setting. The patient's clothes must be removed and isolated, and his or her body washed with soap and water.

Patients with GI exposure should also be decontaminated, but ED staff should not delay urgent treatment with excessive decontamination, given that nosocomial poisoning from GI exposure is rare and controversial. Case reports have described nosocomial poisoning in staff members treating patients who have been exposed to OPCs and carbamates [7, 19, 20] ; one describes OPC toxicity from mouth-to-mouth resuscitation. [21] Only one case discusses serious poisoning in which a staff member required treatment and eventual intubation. [22]

However, none of these cases was confirmed with diagnostic studies. In addition, nosocomial OPC poisoning has not been reported in developing countries with a high incidence of severe OPC poisoning. Moreover, the odors often smelled when one cares for a patient poisoned from pesticide are commonly due to the hydrocarbon solvent, which may cause symptoms independent of the OPC agent. [23]

GI decontamination

Oral administration of activated charcoal is a reasonable intervention after GI poisoning. However, as with any poisoned patient, the risks and benefits must be weighed.

Although a systematic review did not find any clear evidence supporting gastric lavage, the authors recommend lavage in patients who present early after ingestion and have no vomiting, and in patients who require intubation due to acute ingestion of an OPC or carbamate. [24]


Atropine is a pure muscarinic antagonist that competes with ACh at the muscarinic receptor. Most sources recommend starting atropine on patients with anything more than ocular effects and then observing the drying of secretions as an endpoint in titrating to the appropriate dose.

Atropine is most commonly given in intravenous (IV) form at the recommended dose of 2-5 mg for adults and 0.05 mg/kg for children, with a minimum dose of 0.1 mg to prevent reflex bradycardia. Atropine may be redosed every 5-10 minutes.

Atropine requirements may vary substantially from patient to patient. Severe OPC poisonings often require hundreds of milligrams of atropine. In one case report, a patient required frequent doses of atropine and was eventually converted to an atropine infusion to a total of 30 g over 5 days. [25] On the other hand, in the Tokyo sarin episode, patients poisoned by nerve agents had modest atropine requirements, with none requiring more than 10 mg.

Atropine does not bind to nicotinic receptors; therefore, it is ineffective in treating neuromuscular toxicity (particularly weakness of respiratory muscles). Those manifestations require oxime antidotal therapy.


The only oxime available in the United States is pralidoxime (2-PAM). OPCs and carbamates bind and phosphorylate one of the active sites of AChE and inhibit the functionality of this enzyme. Oximes bind to the OPC or carbamate, causing the compound to break its bond with AChE. Most of the effects are on the peripheral nervous system because entry into the CNS is limited.

The main therapeutic effect of pralidoxime is predicted to be recovery of neuromuscular transmission at nicotinic synapses. However, oximes also enhance cholinesterase activity at muscarinic sites, decreasing the requirement for atropine. In vitro experiments have shown that oximes are effective reactivators of human AChE inhibited by OPCs. [26]

In some situations, reactivation of inhibited AChE by oximes is likely to be absent or limited when affinity for the particular OP-AChE complex is poor, the dose or duration of treatment is insufficient, the OP persists in the patient and therefore rapid reinhibition of the newly reactivated enzyme occurs, and the inhibited AChE ages.

The degree of reactivation depends on the specific identities and concentrations of the oxime and the OP. [27, 28, 29, 26] Because diethyl-OP–inhibited AChEs reactivate and age notably slower than the dimethyl analogs, they generally require prolonged oxime treatment. [30] The half-lives of aging of dimethyl phosphorylated or diethyl phosphorylated AChE, as determined in isolated human RBCs in vitro, are 3.7 or 33 hours, respectively, and the therapeutic windows (4 times the half-life) are a maximum of 13 or 132 hours, respectively. [31, 32]

Although animal data [32] and observational clinical data [29, 31, 33] suggest regeneration of AChE and improved outcome, only a few randomized controlled studies have been done. One study by Johnson et al was a comparison of pralidoxime 1 g as a bolus, with pralidoxime 12 g as an infusion (no bolus) over 4 days. Mortality rates, need for ventilation, and rates of intermediate syndrome were higher with the infusion group than with the bolus group. [34]

Another study by Cherian et al was a comparison of pralidoxime 12 g given over 3 days with placebo. Results were similar in both groups, with increased rates of mortality, ventilatory support, and intermediate syndrome. [35]

A more recent randomized study by Pawar et al in patients with moderately severe anticholinesterase pesticide poisoning (all patients received initial 2 g bolus dosing of pralidoxime over 30 min) compared continuous pralidoxime infusion of 1 g/h versus pralidoxime 1 g every 4 hours. Patients with the continuous pralidoxime infusion were found to have decreased atropine requirements and decreased need for intubation. [36]

Both the 1-g bolus dose and the 12-g infusion dose fall short of  World Health Organization (WHO)–recommended dosing for adults, which is a bolus of at least 30 mg/kg followed by an infusion of at least 8 mg/kg/h. Pediatric dosing is a 25-50 mg/kg bolus given over 30 minutes then an infusion of 10-20 mg/kg/h. This WHO recommendation is based on the doses known to achieve serum pralidoxime concentration of greater than 4 mg/L, the minimum effective concentration reported in an early study. [37] Randomized controlled studies with oxime therapy at the WHO-recommended doses are needed to further delineate its effectiveness. The WHO protocol for oxime therapy is recommended for any patient with clinically significant poisoning.

Other treatments

Seizures are an uncommon complication of OPC poisoning. When they occur, they represent severe toxicity. As with most seizures of toxic etiology, benzodiazepines are the preferred medication.

The following agents have shown benefit as adjunctive treatment in OPC poisoning, in preliminary studies:

  • Magnesium sulfate [38, 39]
  • Fresh-frozen plasma [40]


Consult a regional poison control center or toxicologist for further recommendations for patient care. Consult a psychiatrist in any intentional or suspected intentional ingestions.



Researchers in Washington State conducted a longitudinal study among agricultural pesticide handlers during the OP/CB spray season (March-July) over a 6-year period. The use of multiple OP/CBs and mixing/loading activities were found to be significant risk factors for butyrylcholinesterase (BuChE) inhibition, and the use of chemical-resistant boots and lockers for personal protective equipment (PPE) storage were found to be protective factors. These findings supported interventions to reduce exposure such as the implementation of engineering controls for mixing/loading activities, requirements for appropriate footwear, and the regular use of lockers for PPE storage. [39]